Ten children with HSP have been studied. Eight of the 10 children were cultured from the nose, throat and rectum for staphylococcus aureas (SA) and Group A beta hemolytic streptococcus (GAS) at presentation. In some of these 8 children, anti-streptococcus antibodies and/or a rapid strep assay were also done. Cultures from 5 of 8 children were positive for SA (4) or GAS (1). In 2 of 5 children, cultures were positive for SA from all 3 sites. In 2 of 8 children with negative cultures, there was other evidence of GAS (anti-strep antibodies or rapid strep positivity). Thus, 7 of 8 children with HSP had evidence of infection with SA or GAS at the time of presentation. The SA isolates from 2 of the 4 children have been analyzed for toxin production. (The other 2 are pending). One isolate was positive for TSST-1 by PCR and the second isolate was positive for both TSST-1 and SEA. Three patients had a normal CD4 and CD8 T cell Vbeta repertoire in peripheral blood, while 7 had abnormalities noted, in particular in the Vbeta 2 and 3 subsets, when compared to healthy controls. AC, TW, and LM showed elevations of CD4 and CD8 Vbeta 3.1, while CR and CP showed elevations of Vbeta 3.1 only in the CD4 subset. LM showed the elevation of Vbeta 3.1 on 2 independent samples drawn 3 weeks apart. In CR, the elevation of Vbeta 3.1 returned to normal, coincident with clinical resolution of HSP and negative cultures. A skin biopsy done of LM's HSP rash showed early leucocytoclastic vasculitis, IgA, C3, fibrin present within blood vesself of the superficial dermis, consistent with HSP. Vbeta analysis showed an elevation of Vbeta 3, compared to healthy control peripheral blood, and, interestingly, a significant elevation compared to LM's peripheral blood. KT showed an elevation of CD4 Vbeta 2. In contrast, LM and AR showed an abnormally low level of CD4 Vbeta 2. Interestingly, while LM showed this low level of Vbeta 2 in the 2 independent samples drawn 3 weeks apart, a sample assayed almost 2 years later (~ 1 year post-remission) showed normal levels of CD4 Vbeta 2. In conclusion, these preliminary data confirm and extend earlier anecdotal data showing an association between infection and HSP. While GAS, in particular, has been associated with HSP (in about 30% of patients), these data suggest that SA may actually show a stronger association (>60% of patients). These data also suggest HSP-associated Vbeta repertoire changes in peripheral blood and involved skin. Of course, these analyses were done on only a few patients and without disease controls. We do not understand the differences between the patients with and without Vbeta abnormalities. In particular, we do not at this time have the requisite bacteriologic or toxin data in order to draw conclusions regarding Vbeta repertoire changes and particular bacterial exotoxins. However, these data lead us to hypothesize that bacterial toxins may play a role in the pathogenesis of HSP, to suggest that children with HSP be thoroughly cultured for SA as well as GAS, and to advocate clinical trials of aggressive antibiosis in children with HSP.